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Abstract Number: 1618

Suppression of IFN-α Production from Systemic Lupus Erythematosus Immune Complexes Via C1 Complex Enzymatic Properties

Jing Yao Leong1, Joo Guan Yeo1, Thaschawee Arkachaisri2 and Jinhua Lu3, 1Children Intensive Care Unit (CICU), KK Women's and Children's Hospital, Singapore, Singapore, 2Rheumatology & Immunology, KK Women's and Children's Hospital, Singapore, Singapore, 3Microbiology Department, National University of Singapore, Singapore, Singapore

Meeting: 2014 ACR/ARHP Annual Meeting

Keywords: antinucleosome antibodies, C1q, Interferons and systemic lupus erythematosus (SLE)

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Session Information

Title: Systemic Lupus Erythematosus - Human Etiology and Pathogenesis: Autoimmune Disease Transition, Disease Subsets and Prediction of Flares, Cytokines and Autoantibodies

Session Type: Abstract Submissions (ACR)

Background/Purpose

Systemic Lupus Erythematosus (SLE) is an autoimmune disease associated with the development of auto-antibodies particularly against nuclear antigens. Previous studies have revealed the possible role of type I interferon, IFN-α , in disease pathogenesis. Notably the formation of immune complexes (auto-antibodies with auto-antigens) can result in the production of IFN-α via Fc receptor signaling. Hereditary homozygous deficiency in the complement protein, C1q has shown a high penetrance of 88-93% in afflicted individuals resulting in disease development. Remarkably it was shown in recent years that C1q has the capacity to suppress immune complex mediated IFN-α production. Considering that in vivo C1q functions as the sensory adaptor in the C1 complex, we compared C1 with C1q in modulating immune complex-mediated IFN-α production from peripheral blood mononuclear cells (PBMCs).

Methods

Serum samples were obtained from 15 SLE patients and assayed for the presence of auto-antibodies (anti-nucleosome) via ELISA. The monocytic U937 cell line was UV-irradiated and the apoptotic supernatant was harvested after 24 hours. The apoptotic supernatant was incubated with SLE sera to form immune complexes. The immune complexes were pre-treated with C1 complex or, as controls, C1q or PBS. Human PBMCs, isolated from healthy donors by Ficoll- Hypaque density centrifugation were treated with the immune complexes for 24 hours and IFN-α production was measured by ELISA. 

Results

After screening 15 SLE patients for anti-nucleosome autoantibodies, 4 patients with disease activity (SLEDAI-2K ≥ 4) and high titer of anti-nucleosome (>60 R units/ml, where clinical cutoff ≥ 20 R units/ml) were selected. SLE sera were incubated with UV-irradiated U937 apoptotic supernatant to form SLE immune complexes. Human PBMCs were stimulated with SLE immune complexes and assayed for IFN-α production. Healthy control serum elicited 86.7 ± 8.0 R units/ml IFN-α (media control was 85.7 ± 3.5 R units/ml) , whereas SLE patient A elicited 674.7 ± 244.3 R units/ml IFN-α, SLE patient B elicited 243.8 ± 37.0 R units/ml IFN-α (p < 0.05), SLE patient C elicited 1115.8± 166.5 R units/ml IFN-α (p < 0.05), and SLE patient D elicited 142.6 ± 7.4 R units/ml IFN-α (p <0.05). SLE patient C immune complexes were treated with C1, C1q or PBS and C1 and C1q showed a dose-dependent inhibition in IFN-α induction (853.2 ± 16.3, 701.1 ± 1.0, 508.4 ± 18.6 and 192.1 ± 16.4 R units/ml respectively) as compared to PBS-treated SLE immune complex (1362.3 ±80.5 R units/ml). Furthermore, it was noted that, at equal molar concentration of C1 and C1q, C1-treated SLE immune complex suppressed immune complex-induced IFN-α production more effectively than C1q-treated immune complex.   

Conclusion

C1 is the natural complex encompassing C1q and C1-treated SLE immune complexes exhibit suppressed IFN-α induction from human PBMCs. C1 appeared to be more potent than C1q in inhibiting immune complex-induced IFN-a production showing corporation among the complement classical pathway in providing enhanced protection against SLE pathogenesis as compared with C1q alone.


Disclosure:

J. Y. Leong,
None;

J. G. Yeo,
None;

T. Arkachaisri,
None;

J. Lu,
None.

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